|Budget Amount *help
¥214,240,000 (Direct Cost : ¥164,800,000、Indirect Cost : ¥49,440,000)
Fiscal Year 2013 : ¥38,870,000 (Direct Cost : ¥29,900,000、Indirect Cost : ¥8,970,000)
Fiscal Year 2012 : ¥38,870,000 (Direct Cost : ¥29,900,000、Indirect Cost : ¥8,970,000)
Fiscal Year 2011 : ¥41,730,000 (Direct Cost : ¥32,100,000、Indirect Cost : ¥9,630,000)
Fiscal Year 2010 : ¥40,690,000 (Direct Cost : ¥31,300,000、Indirect Cost : ¥9,390,000)
Fiscal Year 2009 : ¥54,080,000 (Direct Cost : ¥41,600,000、Indirect Cost : ¥12,480,000)
In this study, we investigated novel molecular mechanisms underlying the metabolic syndrome, especially focusing on "homeostatic inflammation" that consists of pathogen sensors and their endogenous ligands. We have already demonstrated that the saturated fatty acid-TLR4 pathway plays an important role in the pathophysiology of obesity-induced adipose tissue inflammation. In addition, our data show that ATF4 and ATF3, metabolic stress-induced transcription factors, positively and negatively regulate the TLR4 pathway, respectively. Moreover, Mincle, a pathogen sensor that selectively expressed in macrophages from obese adipose tissue, is a novel regulator of adipose tissue inflammation.